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. Author manuscript; available in PMC: 2014 Apr 24.
Published in final edited form as: J Immunol. 2008 Apr 15;180(8):5662–5669. doi: 10.4049/jimmunol.180.8.5662

FIGURE 1.

FIGURE 1

a, PGP acted via a CXCR-dependent mechanism to cause neutrophil chemotaxis: PMN are pretreated with CXCR1 and CXCR2 Abs or IgG2a isotype control Ab (2 μg/ml) for 1 h at 22°C. PGP (at 10 μg/ml) is placed in the bottom of chemotaxis plate. The isotype Ab demonstrated no change in neutrophil chemotaxis compared with untreated cells (■). However, at 1 μg/ml concentration of each CXCR Ab, PGP chemotaxis is completely blocked (*, p < 0.01 compared with no Ab and isotype Ab control). b, N-α-PGP is increased in CF samples compared with normal control samples: CF (n = 10) and normal control (n = 10) sputum samples were analyzed using ESI-LC/MS/MS for N-α-PGP detection. CF samples demonstrated 8 (80%) of 10 positive for N-α-PGP vs normal controls having 1(10%) of 10 positive for N-α-PGP. The threshold for positivity (0.825 ng/ml) was determined as two SDs above mean (95% confidence interval) for control sputum values.